definitions naming benign vs. malignant hallmarks of cancer introduction to cancer
TRANSCRIPT
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DEFINITIONSNAMING
BENIGN VS. MALIGNANTHALLMARKS OF CANCER
Introduction to Cancer
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Define Neoplasm
Abnormal growth of cells which persists after initial stimulus has been removed
Or Cell growth which has escaped from normal
regulatory mechanisms
Is it benign or malignant? - Can be either!
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Define Benign Neoplasm
Cells which grow as a compact mass and remain at the site of origin
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Define Malignant Neoplasm
Growth of cells is uncontrolled Cells can spread to surrounding tissue
and to distant sites
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Define Dysplasia
Pre-Malignant Condition Describes:
Increased Cell Growth Altered Differentiation Cellular Atypia Common Sites = Cervix, Bladder, Stomach and
Oesophagus
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Define Differentiation
The degree of similarity of tumour cells to the structure of the organ from which the tumour arose
Well differentiated cancer cells look more like normal cells and tend to grow and spread more slowly (low grade)
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Benign Malignant
No invasion No metastasis Retains functionVariable growth
rate, often low
InvadesMetastasises Lose functionVariable growth
rate, may be high
Describe the Behaviour of Neoplasms
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Benign Malignant
CapsuleWell defined edge
Ill-defined marginHaemorrhageNecrotic Centre
Can you describe the Macroscopic differences of neoplasms
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Benign Malignant
Low mitotic count, normal mitoses
Retention of specialisation
OrganisedStructural
differentiation retained
Low to high mitotic count, abnormal mitoses
Loss of specialisation
UnorganisedStructural
differentiation has wide range of changes
Can you describe the Microscopic differences of neoplasms
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What are the 10 Hallmarks of Cancer?
Oncology at a Glance, First Edition. Graham G. Dark. © 2013 John Wiley & Sons, Ltd. Published 2013 by John Wiley & Sons, Ltd.
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10 Hallmarks of Cancer Mnemonic
Immune System Evasion
Invasion and Metastasis
Inducing Angiogenesis
Genomic Instability
Tumour-promoting Inflammation
Metabolism Reprogramming
Sustaining Proliferative Signalling
Replicative Immortality
Resisting Apoptosis
Growth Suppressor Evasion
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Genomic InstabilityMetabolism Reprogramming
Multistep genetic mutations occur, each enabling further clonal expansion of pre-malignant cells
In cancer cells, the accumulation of mutations goes unchecked and therefore, these cells are more sensitive to mutagenic actions
To sustain proliferation, cancer cells make adjustments to their energy production by: Reprogramming their
glucose metabolism Upregulating glucose
transporters such as glucose transporter 1 (GLUT1)
Depending on alternate metabolic pathways
What Happens First?
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Sustaining Proliferative Signalling
Growth Suppressor Evasion
Healthy tissues regulate growth-promoting signaling pathways, which are responsible for driving progression of cells through the cell cycle.
These signaling mechanisms are deregulated in cancerous cells.
Tumour suppressors (Rb and TP53) halt cell cycle progression if excessive genome damage occurs
Cancer cells are able to proliferate independantly of these signals
How Does It Survive?
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Replicative ImmortalityTumour Promoting Inflammation
Normal cells are able to divide a finite no. of times and then cell division is blocked
Cancer cells overcome this by over-expressing telomerase, an enzyme that maintains telomere length, which protects the ends of chromosomes and allows the cell to continue proliferating.
Tumour-associated inflammation may aid in tumour growth by supplying the tumour microenvironment with: Growth Factors Pro-Angiogenic Factors Survival Factors
How Does It Survive?
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Resisting Apoptosis Immune System Evasion
All cancer cells dysregulate 2 signalling pathways by:1. Overexpressing anti-
apoptotic proteins2. Silencing pro-apoptotic
proteins Also resist cell death by
altering normal cellular autophagy and necrosis
How Does It Survive?
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Invasion and Metastasis Inducing Angiogenesis
Infiltration of nearby blood and lymphatic vessels
Cancer cells are transported to non-contiguous tissues (forming metastatic lesions)
Development of new blood vessels
All cancers require a vascular network to supply nutrients and remove waste
VEGF and PDGF are key players
How Does It Thrive?